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Biomedical subjects

P Layer

Publications and source records attributed to P Layer.

At least 145 records · Page 8Linked to original sources
PubMed1986

[Tuberculostatics-induced systemic lupus erythematosus].

Clinical manifestations including rheumatoid changes, lymph node swelling, fever, butterfly rash, anaemia and leukopenia had developed gradually over a period of years in a 46-year-old female patient. Due to these findings systemic lupus erythematosus (SLE) was suspected. Further diagnostic procedures revealed concomitant pulmonary tuberculosis. In the course of the tuberculostatic therapy, there occurred six episodes of marked exacerbation of drug-induced SLE signs and symptoms including fever, myalgia, swelling of joints, butterfly rash and high titers of antinuclear antibodies. These exacerbations were induced by single-agent or combination therapy with ethambutol, pyrazinamide, streptomycin and/or prothionamide and resolved readily after discontinuation of the drug(s). With concomitant use of hydroxychloroquine sulfate, a combination therapy with rifampicin and cycloserine did not give rise to further complications although the autoantibodies persisted. This treatment regimen was given until clinical cure was achieved.

Antitubercular Agents↗
PubMed1986

Gastroparesis after radiation. Successful treatment with carbachol.

Following abdominal radiation, a 16-year-old male developed persistent vomiting, metabolic alkalosis, and cachexia secondary to gastric stasis, atony, and dilatation in the absence of mechanical obstruction. Fluoroscopically and manometrically, antral motility was found to be severely impaired. Antral motor activity was not influenced by metoclopramide, but stimulated by carbachol. During oral maintenance carbachol therapy, gastric emptying of food was restored and sufficient oral nutrition could be resumed. The improvement persisted even after termination of therapy four months later. Systematic investigations on the effects of abdominal radiation on gastrointestinal motility appear to be necessary.

Adolescent↗
PubMed1986

Bile secretion in acute and chronic hypercalcemia in the cat.

The reported coincidence of primary hyperparathyroidism and cholelithiasis led us to investigate the effects of acute and chronic hypercalcemia on bile secretion in cats. Acute hypercalcemia (6-7 mmol/liter) was induced by an intravenous calcium infusion. Chronic hypercalcemia (3-4 mmol/liter) was induced and maintained for 8-10 weeks by treatment with subcutaneous vitamin D3, oral dihydrotachysterol, and feeding a calcium-rich diet. Bile secretion was then studied in acute experiments. We found that calcium concentrations in serum and hepatic bile were similar during all experimental normo- or hypercalcemic conditions (y = 1.12x - 0.85; r = 0.76). Biliary volume outputs were significantly decreased during both acute (P less than 0.002) and chronic (P less than 0.05) hypercalcemia compared with normocalcemic controls. Acute hypercalcemia also decreased total bile acid outputs (P less than 0.05), but had no effect on biliary bile acid concentrations. The inhibitory effect of acute hypercalcemia on biliary fluid and bile acid secretion was dose dependent and not antagonized by atropine. These findings suggest that calcium is secreted in hepatic bile at similar concentrations as present in the serum and that elevations of serum calcium concentration inhibit biliary volume and bile acid secretion in cats. Similar effects of hypercalcemia on bile composition in humans might promote calcium salt precipitation in bile.

Acute Disease↗
PubMed1986

Effects of decreasing intraluminal amylase activity on starch digestion and postprandial gastrointestinal function in humans.

We used an amylase inhibitor preparation that markedly improves postprandial carbohydrate tolerance in humans to investigate the effects of decreased intraluminal amylase activity on digestion of starch and postprandial gastrointestinal and hormonal responses. Four fasting volunteers were intubated with an oroileal tube to obtain duodenal, jejunal, and terminal ileal samples. After intubation, subjects ingested 50 g of rice starch given with placebo; on the second day, starch was given with the amylase inhibitor. Compared with placebo, the amylase inhibitor significantly (p less than 0.05) reduced duodenal, jejunal, and ileal intraluminal amylase activity by more than 95% for 1-2 h; increased postprandial delivery of total carbohydrate (glucose polymers in particular) to the distal small bowel; increased breath hydrogen concentrations; decreased intestinal water absorption and increased distal intestinal volume delivery to the distal bowel; shortened duodenoileal transit time but doubled postprandial gastric emptying time; reduced the early postprandial plasma glucose rise by 85% and eliminated the late postprandial glucose fall to below fasting levels; and abolished postprandial plasma concentrations of insulin, C-peptide, and gastric inhibitory polypeptide. Postprandial trypsin output was not influenced. We conclude that more than 95% inhibition of amylase reduces dietary starch digestion within the small intestine and uptake of dietary starch from the small intestine, markedly decreases postprandial release of insulin and gastric inhibitory polypeptide, and may alter postprandial upper gastrointestinal motor function.

Adult↗
PubMed1986

Effect of a purified amylase inhibitor on carbohydrate tolerance in normal subjects and patients with diabetes mellitus.

Slowing starch digestion by inhibiting amylase activity in the intestinal lumen should improve postprandial carbohydrate tolerance in patients with diabetes mellitus. Crude bean-derived amylase inhibitor ("starch blocker") that contains only minimal antiamylase activity, however, does not modify carbohydrate assimilation. To test the validity of the "starch blockade" concept, we assessed the effect of a partially purified bean-derived amylase inhibitor with increased antiamylase activity on carbohydrate tolerance in normal subjects and in patients with non-insulin-dependent diabetes mellitus. In comparison with a placebo, ingestion of this inhibitor with 50 g of starch substantially reduced postprandial increases in plasma concentrations of glucose and insulin in both normal subjects and those with diabetes. We conclude that a purified amylase inhibitor is effective and potentially beneficial in the treatment of diabetes mellitus.

Adult↗
PubMed1986

Stimulatory effect of hypercalcemia on pancreatic secretion is prevented by pretreatment with cholecystokinin and cholinergic agonists.

Recently, we demonstrated that hypercalcemia causes marked stimulation of feline exocrine pancreatic secretion, and that this effect is absent when a large dose of cholecystokinin (CCK) is infused prior to induction of hypercalcemia. To investigate this effect in more detail, anesthetized cats were given calcium i.v. after preadministration of CCK or urecholine (a cholinergic agonist) at specific doses, or of saline as a control. We found that the hypercalcemia-induced stimulation of pancreatic protein secretion was abolished after preadministration of CCK at large doses. After the prestimulus dose was decreased or the calcium dose was increased, however, the pancreatic secretory response to hypercalcemia was preserved. In contrast, the response to a submaximal dose of CCK was unchanged after prestimulation with a large dose of CCK. Similar results were obtained when urecholine instead of CCK was used as prestimulus. These findings indicate that loss of pancreatic responsiveness to hypercalcemia following prestimulation with CCK is dependent on doses of both prestimulus and calcium used, and that it is not specific for prestimulation with CCK but also inducible by cholinergic agonists. They further suggest that this phenomenon is not due to exhaustion of pancreatic secretory capacity, but may reflect decreased sensitivity to the hypercalcemic stimulus instead.

Animals↗
PubMed1986

Fate of pancreatic enzymes during small intestinal aboral transit in humans.

To determine survival of pancreatic enzymes during small intestinal aboral transit in humans, seven healthy volunteers were intubated with an oroileal tube. By using nonabsorbable markers we measured the cumulative amount of lipase, trypsin, and amylase activities and lipase and trypsin immunoreactivities delivered postprandially to the duodenum, midjejunum, and terminal ileum. We found that as the enzymes moved from duodenum to ileum, 74% of amylase activity, 22% of trypsin activity, and 1% of lipase activity survived transit. Enzymatic activity and immunoreactivity of trypsin and lipase disappeared at different rates, suggesting that for these enzymes the sites of enzymatic activity and immunorecognition are not identical. Since tryptic activity is present even in the absence of immunorecognizable trypsin, complete structural integrity of the trypsin molecule may not be essential for its enzymatic activity. The short intraluminal survival of lipolytic activity may partially explain why patients with progressive exocrine pancreatic insufficiency malabsorb fat earlier than other nutrients.

Adult↗
PubMed1986

Duodenal calcium in chronic pancreatitis: is it of diagnostic value?

Chronic pancreatitis has been reported to be associated with an increased secretion of calcium in pancreatic juice. To determine whether estimation of duodenal calcium may be useful for diagnosing chronic pancreatitis, we compared duodenal calcium output in patients with chronic pancreatitis and in subjects without pancreatic disease, during intravenous infusion of secretion alone, with calcium, or with cholecystokinin-pancreozymin (CCK-PZ). Duodenal calcium output increased during infusion of both calcium and CCK-PZ to a similar extent in chronic pancreatitis and controls. Overall, duodenal output of chymotrypsin was markedly lower in chronic pancreatitis; however, chymotrypsin output increased in response to both intravenous calcium and CCK-PZ in both groups. Bilirubin output increased in both groups during calcium infusion, but this increase was significantly reduced in chronic pancreatitis; in contrast, CCK-PZ caused a similar increase in both groups. The high calcium output observed in hypercalcemia in the presence of low enzyme output suggests increased pancreatic secretion of enzyme-independent calcium in chronic pancreatitis. However, the difference is obscured by biliary calcium, which is secreted in much higher concentrations. Thus, duodenal calcium determination does not appear to be a useful diagnostic test in chronic pancreatitis.

Bilirubin↗
PubMed1986

Bile-stimulated secretin release in cats.

Duodenal perfusion with sodium taurocholate (TC), pH 10.5 (60 mM, made isotonic with NaCl, 30 ml/h for 90 min), increased the plasma immunoreactive secretin level (IRS) from 2.1 +/- 1.0 to 19.1 +/- 6.0 pM (p less than 0.025; n = 6) in anaesthetized cats. Dose-response studies with TC, pH 7.2 (0-60 mM, made isotonic with NaCl, 45 ml/h for 20 min), demonstrated a threshold concentration of TC for IRS release between 10 and 15 mM (p = 0.05; n = 6). Instillation of gallbladder bile from the same animal (1.5 +/- 0.1 ml, pH 7.0 +/- 0.1, over 12 min) increased the IRS concentration from 1.5 +/- 0.4 to 8.1 +/- 3.4 pM (p less than 0.025; n = 6). IRS concentrations also increased when gallbladder bile was mixed with either saline (from 3.4 +/- 1.7 to 11.6 +/- 2.5 pM; p less than 0.05; n = 5) or feline pure pancreatic juice (PPJ) (from 3.1 +/- 0.7 to 5.7 +/- 1.1 pM; p less than 0.025; n = 6). The peak value was significantly lower when bile was mixed with PPJ than with saline (p less than 0.05). We conclude that TC, the dominating bile salt in feline bile, can release IRS also above pH 7, that physiological concentrations of TC can elicit this response, that the response is also produced by gallbladder bile from the same animal, and that PPJ inhibits the bile-induced IRS release. Thus secretin release by bile is likely to be a physiological principle in the regulation of the pancreatic secretion.

Animals↗
PubMed1985

Partially purified white bean amylase inhibitor reduces starch digestion in vitro and inactivates intraduodenal amylase in humans.

Whether commercial, bean-derived alpha-amylase inhibitor preparations failed to decrease starch digestion in humans because of insufficient antiamylase activity, destruction by gastrointestinal secretions, or decreased activity in the presence of starch is unknown. We used a simple partial purification procedure to markedly concentrate the inhibitor (sixfold to eightfold by total protein content, and 30-40-fold by dry weight). Compared with a commercial preparation and crude bean extract, this partially purified inhibitor inactivated intraduodenal, intraileal, and salivary amylase in vitro faster and more completely (p less than 0.001); its specific activity was not affected by exposure to gastric juice and was only minimally reduced by duodenal juice. Whereas the rate of amylase inhibition by inhibitor was markedly slowed in the presence of nondietary liquid starch, dietary solid starch had only a minimal effect. Consequently, the partially purified inhibitor had no effect on liquid starch digestion, but decreased in vitro digestion of dietary starch in a dose-dependent manner (p less than 0.001). Perfusion of the partially purified inhibitor (2.0, 3.5, or 5.0 mg/ml at 5 ml/min) into the duodenum of humans rapidly inhibited greater than 94%, greater than 99%, or greater than 99.9% of intraluminal amylase activity. We conclude that commercial amylase inhibitors failed to decrease starch digestion in vivo mainly because they have insufficient antiamylase activity. However, a partially purified inhibitor with increased specific activity is stable in human gastrointestinal secretions, slows dietary starch digestion in vitro, rapidly inactivates amylase in the human intestinal lumen, and, at acceptable oral doses, may decrease intraluminal digestion of starch in humans. Such an inhibitor therefore deserves study.

Adult↗
PubMed1985

Effects of acute hypercalcemia on exocrine pancreatic secretion in the cat.

To investigate the effects of acute hypercalcemia on exocrine pancreatic secretion, anesthetized cats were given calcium intravenously. Increasing hypercalcemia (3.7-6.3 mmol/L) evoked a dose-dependent increase in enzyme output that was 12 times greater than in normocalcemic controls (p less than 0.001) and was 60% of subsequent maximal stimulation with intravenous cholecystokinin (CCK). The effect of hypercalcemia on enzyme secretion was abolished when CCK was administered 60 min before calcium and at a dose to cause maximal enzyme output. Atropine did not prevent the calcium-induced increase in enzyme secretion. Pancreatic fluid and bicarbonate outputs were not influenced by hypercalcemia during intravenous administration of small amounts of secretin, but were increased by addition of CCK to the secretin infusion. Hypercalcemia did not induce macroscopic or light-microscopic changes in pancreatic morphology. Plasma levels of both CCK and gastrin were increased (p less than 0.01) during hypercalcemia, with and without precalcium administration of CCK; atropine significantly inhibited (p less than 0.05), but did not abolish the calcium-induced releases of both peptides. These data suggest that in the anesthetized cat, acute hypercalcemia induced by intravenous calcium infusion stimulates pancreatic secretion of enzymes, but not fluid and bicarbonate. Acute hypercalcemia also causes release of CCK and, as shown previously, gastrin. The findings suggest that the stimulatory effect of hypercalcemia on pancreatic enzyme secretion is not dependent on intact cholinergic pathways and is probably not exclusively mediated by release of CCK or gastrin.

Acute Disease↗
PubMed1985

Hereditary pancreatitis. Presentation of an additional family.

A West German family with hereditary pancreatitis is described. Four members are definitely known to have had pancreatitis, while three additional members are suspected of having the disease. The mean age of onset of symptoms was 14 years. Known causes of secondary pancreatitis and amino aciduria were ruled out in each case. HLA-segregation was analysed on the A, B, C, and DR loci in all members of the family, but no coupling between distribution of HLA haplotypes and incidence of pancreatitis was detected.

Adult↗
PubMed1985

[Severe malabsorption syndrome and exudative enteropathy in hypogammaglobulinemia: complete involution with intravenous immunoglobulin substitution].

A 35 year old woman with primary hypogammaglobulinaemia developed intestinal villous atrophy, a severe malabsorption syndrome, osteomalacia and protein-losing enteropathy. The syndrome did not respond to treatment with antibiotics, vitamins, or gluten free diet. Regular intravenous administration of a native immunoglobulin preparation induced continuous elevation of IgG serum levels above 240 mg/dl. This led to rapid, complete and persistent normalisation of all clinical symptoms and pathologic findings. Additional therapy was not required. Side effects of the treatment that has now been maintained for 48 months were not observed.

Adult↗